LitCovid-sentences  

PMC:7381711 / 4888-8075 JSONTXT 11 Projects

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Id Subject Object Predicate Lexical cue
T35 0-39 Sentence denotes COAGULOPATHY AND THROMBOSIS IN COVID-19
T36 40-122 Sentence denotes Many patients with COVID-19 develop a clinically significant coagulopathy (7, 32).
T37 123-377 Sentence denotes The coagulopathy associated with COVID-19 is characterized by thrombocytopenia, minor prolongation of prothrombin time (PT) and partial thromboplastin time (aPTT), and elevated serum D-dimer and fibrinogen, consistent with a consumptive coagulopathy (7).
T38 378-668 Sentence denotes This profile is compatible with postmortem examinations of patients with COVID-19 describing severe endothelial injury, microangiopathy, and alveolar capillary microthrombi (2) Endotheliitis directly elicited by SARS-CoV-2 may be the pathophysiologic link to these postmortem findings (39).
T39 669-907 Sentence denotes In addition to laboratory and histopathological evidence of disordered coagulation and endothelial injury, several reports suggest that patients with COVID-19 are at high risk for developing clinically significant large-vessel thrombosis.
T40 908-1258 Sentence denotes Early anecdotal evidence of venous thromboembolism (VTE) in critically ill patients has been confirmed by multiple case series describing high rates of VTE in COVID-19, with incidence estimates ranging between 8% and 54% (18, 22), significantly exceeding those reported in critically ill patients with H1N1 influenza of 2% (36) and sepsis of 5% (30).
T41 1259-1402 Sentence denotes Reports of large-vessel strokes in patients, including those younger than 50 yr, infected with SARS-CoV-2 also suggest hypercoagulability (28).
T42 1403-1564 Sentence denotes Concordantly, a postmortem study of 12 patients positive for COVID-19 found thrombosis in 58% of cases, which was found to be responsible for 25% of deaths (45).
T43 1565-1704 Sentence denotes Taken together, it is likely that COVID-19-associated coagulopathy and thromboses contribute to the morbidity and mortality of the disease.
T44 1705-1924 Sentence denotes However, it is important to recognize that other non-COVID-19 critical illnesses have demonstrated similar evidence of coagulopathy, yet failed to benefit from anticoagulation treatment in randomized controlled studies.
T45 1925-2169 Sentence denotes For example, coagulopathy has been widely recognized as a contributor to organ failure in sepsis, a disease characterized by circulating D-dimer concentrations that approximate levels observed in patients with COVID-19 (Fig. 2; 10, 32, 38, 40).
T46 2170-2427 Sentence denotes However, studies that have targeted this coagulopathy in sepsis with thrombomodulin (40), AT3 (42), tissue factor pathway inhibitor (1), and activated protein C (31) have all failed to improve mortality, despite improving laboratory indexes of coagulopathy.
T47 2428-2556 Sentence denotes These studies suggest that coagulopathy may simply be a consequence of sepsis, as opposed to a key pathogenic driver of disease.
T48 2557-2743 Sentence denotes Alternatively, as discussed below, coagulation may impart both harmful and protective effects within the injured lung, negating any clinical benefit (or harm) from anticoagulant therapy.
T49 2744-2751 Sentence denotes Fig. 2.
T50 2753-2826 Sentence denotes Coagulopathy in sepsis compared with coronavirus disease 2019 (COVID-19).
T51 2827-2966 Sentence denotes Circulating levels of D-dimer, a marker of coagulopathy, have been found to be significantly and similarly elevated in sepsis and COVID-19.
T52 2967-3021 Sentence denotes This panel represents medians and interquartile range.
T53 3022-3030 Sentence denotes Studies:
T54 3031-3118 Sentence denotes Bernard et al. (10), Vincent et al. (40), Tang et al. (38), and Richardson et al. (32).
T55 3119-3187 Sentence denotes NYC, New York City; pts, patients; RCT, randomized controlled trial.